GM-CSF induces human neutrophil IgA-mediated phagocytosis by an IgA Fc receptor activation mechanism

RH Weisbart, A Kacena, A Schuh, DW Golde - Nature, 1988 - nature.com
RH Weisbart, A Kacena, A Schuh, DW Golde
Nature, 1988nature.com
Immunoglobulin A is the primary immunoglobulin isotype in tears, saliva, breast milk and
other mucosal secretions, constituting between 6% and 15% of the total serum
immunoglobulins1. Human peripheral blood neutrophils have IgA receptors, but these cells
do not normally participate in IgA-mediated phagocytosis. The haematopoietic factors
granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-
stimulating factor (G-CSF) prime neutrophils to be more responsive to a variety of stimuli2–4 …
Abstract
Immunoglobulin A is the primary immunoglobulin isotype in tears, saliva, breast milk and other mucosal secretions, constituting between 6% and 15% of the total serum immunoglobulins1. Human peripheral blood neutrophils have IgA receptors, but these cells do not normally participate in IgA-mediated phagocytosis. The haematopoietic factors granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) prime neutrophils to be more responsive to a variety of stimuli2–4. We therefore studied their effect on IgA-mediated phagocytosis. GM-CSF and G-CSF both induce a change from low to high-affinity neutrophil IgA Fc crystallizable fragment receptors within 30min; a change which is associated with the development of IgA-mediated phagocytosis. Human IL-3, which does not affect neutrophil function, is inactive in this sytem. These results define a new mechanism for CSF-agumented host defence whereby neutrophil function can be modulated by CSF-mediated IgA Fc receptor activation.
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